Patients with major thermal injuries rarely proceed to recovery without sepsis; even with early excision, vigorous antibiotic therapy, and prompt closure of burn wounds by skin grafting. Indeed, since the introduction of modern fluid resuscitation methods and respiratory care techniques, sepsis is now recognized as the primary cause of death following thermal injury. An association between the occurrence of sepsis and the occurrence of spontaneous immunosuppression has often been recognized in burn patients. Most often, this association is described as causative, that is, the suppression caused by the injury results in increased risk of sepsis. It is our conviction, however, that the opposite association may be even more important, and that endotoxin (and, perhaps, endotoxin-like molecules) are responsible for the immune suppression which follows thermal injury. It is the purpose of this study to determine if bacterial endotoxins produced by endogenous as well as exogenous microorganisms are capable of generating suppressor effects which, under the proper conditions, are great enough to promote sepsis and/or allograft survival as seen following thermal injury. In addition, the ability of endotoxin-like "cutaneous burn toxin" to produce such effects will also be evaluated. In vitro methodology will include MLC and PHA cultures of normal human lymphocytes, utilized to evaluate suppression, the generation of suppressor cells, and the blocking of such effects by antibody or dissociation of endotoxin by bile treatment. In vivo evaluation will be accomplished both in humans (with the cooperation of the Department of Medicine at Utah) and in inbred mouse models.